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conferenceseries.com
Volume 08 Journal of Alzheimers Disease & Parkinsonism Alzheimer's Congress 2018
May 30-31, 2018
May 30-31, 2018 Osaka, Japan
10th World Congress on
Alzheimer's Disease & Dementia
Regulator of G-protein signaling 10modulates neuroinflammation andmetabolic homeostasis:Apotential
role in alzheimer’s diseases
Jae-Kyung Lee
University of Georgia, USA
Insulin resistance and aging-related metabolic disorders constitute serious threats to human health as risk factors for
Alzheimer’s Disease (AD); especially impaired brain glucose homeostasis was related to the severity of the AD pathology.
Regulator of G-protein Signaling proteins (RGSs) are a family of proteins that negatively regulate G-Protein Coupled Receptors
(GPCR) through their GTPase Accelerating Protein (GAP) activity. RGS10 is one of the smallest RGS family proteins which we
have shown to negatively regulate microglia activation and the level of RGS10 in microglia significantly decreased within the
microglia by age. RGS10-deficient microglia displayed impaired phagocytic activity to amyloid-beta fibrils (fAβ). Interestingly,
RGS10-deficient mice spontaneously gained weight with age (>15 months) and the level of RGS10 protein was decreased
in postmortem brains of the AD and Frontal Temporal Dementia (FTD). Our data demonstrate that RGS10-deficient mice
display impaired glucose tolerance, the high level of triglycerides (TG) in plasma. RGS10-deficient mice spontaneously gained
weight with age (>15 months). We also tested whether RGS10 plays a role in high-fat-induced chronic inflammation and
glucose metabolism as a risk factor for metabolic disorder in the periphery and the CNS. Indeed, HFD-fed RGS10-deficient
mice gained significantly more weight compared to HFD-fed wild-type (WT) mice. Importantly, HFD-fed RGS10-deficient
mice displayed an insulin resistance phenotype and impaired Long-Term Potentiation (LTP). These data implicate RGS10 may
play a critical role of in insulin sensitivity during metabolic disorders in the periphery and the CNS. Importantly, peripheral
metabolic disorders, including obesity and insulin resistance along with chronic inflammation have been shown to contribute
to development and progression of cognitive impairment and alzheimer’s disease through multiple mechanisms. Our data
strongly implicate the role of RGS10 inmodulating metabolic homeostatsis related to its role in neuroinflammation. Elucidating
RGS10 function in maintaining metabolic homeostasis in the CNS and periphery may provide the mechanism to link aging
associated chronic inflammation and metabolic disorders, which could be a potential therapeutic target for alzheimer’s diseases
with dual effects on both inflammation and metabolic disruption. Overall, our study produced highly novel data delineating
potential mechanisms of RGS10 function in metabolic homeostasis in the brain.
Biography
Jae-Kyung Lee has completed her PhD in UNT Health Science Center and Postdoctoral studies from UT Southwestern Medical Center at Dallas. She had worked
as an Assiatant Professor at Emory University until 2015. Currently, she is an Assistant Professor in University of Georgia, USA. She has published more than 24
papers in reputed journals. Her research focused on understanding how inflammation influences neurodegenerative diseases.
Jae-Kyung Lee, J Alzheimers Dis Parkinsonism 2018, Volume 8
DOI: 10.4172/2161-0460-C4-046